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  • Title: Does remodeling occur in the diseased human saphenous vein bypass grafts? An intravascular ultrasound study.
    Author: Ge J, Liu F, Bhate R, Haude M, Görge G, Baumgart D, Sack S, Erbel R.
    Journal: Int J Card Imaging; 1999 Aug; 15(4):295-300. PubMed ID: 10517379.
    Abstract:
    BACKGROUND: Coronary artery remodeling is a common phenomenon in human atherosclerotic arteries. Controversies exist concerning the presence of absence of the remodeling process in diseased human coronary saphenous vein bypass grafts. The purpose of the study was to observe the vessel and lumen dimensions in patients who had undergone saphenous vein grafting with intravascular ultrasound to find out whether the remodeling process exists in the diseased human saphenous vein bypass grafts. METHODS: A total of 43 saphenous vein bypass grafts from 43 patients (39 males, 4 females, mean age 63+/-8 years); 1-16 years (mean 9.3+/-4.0 years) after grafting, who had not undergone previous catheter intervention, were studied using intravascular ultrasound. The vessel, lumen and plaque area were measured at the lesion segment as well as in the proximal and distal reference segments. The percent stenosis was calculated. RESULTS: In 43 bypass grafts having severe stenosis before intervention, plaque was eccentric in 69.4% and concentric in 30.6%. No calcification was detected in 75% cases and 25% cases has mild-moderate intimal calcification. The vessel area in the lesion segment was 19.0+/-9.7 mm2, significantly larger than the proximal reference segment 12.8+/-4.0 min2 as well as the distal reference segment 12.9+/-3.6 mm2 (p < 0.001). It was also larger than that of the average area of the proximal and distal reference segments (p < 0.001). The vessel area increased in accordance with plaque area (p < 0.001). A weak relationship existed between vessel area and percent stenosis (r = 0.37, p = 0.04). CONCLUSION: In contrary to previous findings, diseased human saphenous vein bypass grafts undergo focal compensatory enlargement (remodeling) in the presence of plaque formation. The underlying mechanism is probably similar to that in de novo atherosclerosis.
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